Retinal rods utilize a prototypical G-protein signaling cascade to encode our visual scene under dim light. Over-stimulation of this cascade by bright light, or genetic mutations that act as equivalent light, are known environmental factors that exacerbate disease progression for age-related macular degeneration (AMD) as well as other retinal disorders in humans. Although it is known that rhodopsin activation is required for light-induced pathogenesis, the distinct molecular pathways remain to be defined. The first two aims will investigate biochemical reactions in rods that may slow dark adaptation following bright light exposure. The third aim will investigate two different mechanisms of light-induced rod cell death. The long-term objective of this proposal is to understand phototransduction in normal function and dysfunction so that this knowledge can be used to devise strategies for the treatment of human visual disorders.